Part 84

These lesions may be variously combined with each other. It is to be noted that in the first three varieties protective adhesions are present, and that in the last these adhesions are either absent or ruptured.

When the pancreas, the liver, or the spleen form the floor of the ulcer, they may be protected from extension of the ulcerative process by a new growth of fibrous tissue extending from the floor of the ulcer a variable depth into these organs. Sometimes, however, the ulcerative process, aided doubtless by the corroding action of the gastric juice, eats out large excavations in these organs. These excavations communicate with the cavity of the stomach, and are usually filled with ichorous pus. The pancreas, unlike the spleen and the liver, possesses comparative immunity against this invasion by the ulcerative process.

The situation, the form, and the extent of circumscribed peritoneal abscesses resulting from perforation of gastric ulcer depend upon the parts with which the stomach has contracted adhesions. Should an ulcer on the posterior wall of the stomach perforate before the formation of adhesions, the perforation would of course be directly into the lesser peritoneal cavity. An interesting example of this rare occurrence has been communicated by Chiari. In this case, the foramen of Winslow being closed by adhesions, the lesser peritoneal cavity which communicated with a gastric ulcer was filled with ichorous pus, and in this floated the pancreas, which had necrosed in mass and had separated as a sequestrum. That form of intra-peritoneal abscess known as subphrenic pneumo-pyothorax has been already described under Symptomatology. Peritoneal abscesses communicating with the stomach may open into various places, {508} as into the general peritoneal cavity, into the pleural cavity, into the retro-peritoneal tissue, through the abdominal or thoracic walls, etc.

Gastro-cutaneous fistulæ are a rare result of the perforation of gastric ulcer. The external opening is most frequently in the umbilical region, but it may be in the epigastric or in the left hypochondriac region or between the ribs. Fistulous communications resulting from the perforation of gastric ulcer have been formed between the stomach and one or more of the following hollow viscera or cavities: the colon, the duodenum and other parts of the small intestine, the gall-bladder, the common bile-duct, the pancreatic duct, the pleura, the lung, the left bronchus, the pericardium, and the left ventricle. Gastro-colic fistulæ, in contrast to gastro-cutaneous fistulæ, are more frequently produced by cancer than by ulcer of the stomach. In rare instances the peritoneum over ulcers of the lesser curvature has contracted adhesions with the pyloric portion of the stomach or with the first part of the duodenum. To accomplish this it is necessary that a sharp bend in the lesser curvature should take place. By extension of the ulcerative process abnormal communication is established between the left and the right half of the stomach or between the stomach and the duodenum. In either case the right half of the stomach is often converted into a large blind diverticulum, the digested food passing through the abnormal opening. Gastro-duodenal fistulæ are more frequently with the third than with the first part of the duodenum. In one of Starcke's cases the stomach communicated with the colon and through the medium of a subphrenic abscess with the left lung.

Four cases of perforation of gastric ulcer into the pericardium, with the production of pneumo-pericardium, have been reported, and two cases of perforation into the left ventricle. Müller found lumbricoid worms in a pleural cavity which had been perforated by gastric ulcer. Diaphragmatic hernia may result from perforation of the pleural cavity by gastric ulcer. In one instance the greater part of the small intestines {509} passed through a hole in the transverse meso-colon which had been caused by a gastric ulcer.

The various fistulæ which have been mentioned may be either direct or through the medium of an abscess. While some of them are only pathological curiosities, others, particularly the communications of the stomach with the pleural cavity and with the lung, are sufficiently frequent to be of practical clinical interest.

As has already been explained, ulcers of the anterior wall are the ones most liable to perforate into the general peritoneal cavity, but on account of their comparative infrequency perforation occurs oftener in other situations, particularly in the lesser curvature and near the pylorus. Except on the anterior wall the perforation is often brought about by the rupture of adhesions which for a time had prevented this accident. In a considerable number of cases, particularly of ulcers on the anterior wall, the ulcer looks as if recently formed (acute perforating ulcer); in other cases its thickened and indurated margins indicate long duration. Chiari describes a case in which rupture into the peritoneal cavity took place through the cicatrix of an old ulcer, probably in consequence of the distension of the stomach with gas. The hole in the peritoneum is usually circular, smaller than the inner surface of the ulcer, and has sharp, well-defined edges. Less frequently the edges are ragged. Post-mortem digestion may, however, so change the borders of the opening as to make it difficult or impossible to tell from their post-mortem appearances alone whether perforation has occurred before or after death. The peritoneal cavity after death from perforation is found to contain gas and substances from the stomach. Usually within a few hours after perforation septic peritonitis is excited, but in exceptional cases no inflammation of the peritoneum has occurred even when life has been prolonged twenty-four hours after perforation.

Emphysema of the subcutaneous, subperitoneal, and other loose areolar tissue of the body is a rare but remarkable result of the perforation of gastric ulcer. The emphysema is sometimes observed shortly before death, but it attains its maximum development after death, when it may spread rapidly over the greater part of the body. The gas consists in part of hydrogen, as it burns with a blue flame. It is generated, at least in great part, by fermentation of the contents of the stomach. The gas may enter the subserous tissue at the edges of the ulcer and thence spread, or, after perforation of the stomach, it may make its way from the peritoneal cavity into the loose subserous connective tissue through some place in the parietal peritoneum which has been macerated, perhaps by the digestive action of the gastric juice.

In two cases of sudden death from gastric ulcer Jürgensen found gas in the veins and arteries of various parts of the body. He believes that this gas, which certainly was not the result of putrefaction after death, was derived from the stomach, and that it entered during life the circulation through vessels exposed in the borders of the ulcer, thus causing death. In one of the cases a profuse hemorrhage preceded death, and in the other the ulcer had perforated into the peritoneal cavity.

The source of hemorrhage from gastric ulcer is from blood-vessels either in the stomach itself or in the neighborhood of the stomach. Hemorrhages slight or of moderate severity occur from the capillaries and small arteries and veins in the mucous and submucous coats. Sometimes profuse and even fatal hemorrhage comes from arteries or from veins in the submucous coat, especially when these vessels are dilated. Quickly-fatal hemorrhages take place from the large vessels between the muscular and the serous coats, particularly from the main trunks on the curvatures. After the formation of adhesions, followed by the perforation of all of the coats of the stomach, profuse bleeding may proceed from the erosion of large vessels near the stomach, such as the splenic, the hepatic, the pancreatico-duodenal arteries, the portal and the splenic veins, and the mesenteric vessels. Bleeding may also occur from vessels in the parenchyma of organs invaded by the ulcer. The most common source of fatal hemorrhage is from the splenic artery, which from its position is peculiarly exposed to invasion by ulcers of the posterior wall of the stomach. The hemorrhage is usually arterial in origin. It may come from miliary aneurisms of the gastric arteries or from varicose veins in the wall of the stomach. As Cruveilhier has pointed out, an ulcer may cicatrize except over one spot corresponding to an artery from which fatal hemorrhage may occur. Ulcers which give rise to large hemorrhages are usually chronic in their course. Those seated on the middle of the anterior wall, although peculiarly liable to perforate, are comparatively exempt from hemorrhage on account of the small size of the blood-vessels there.

Changes in the blood-vessels of the stomach have been seen in a considerable number of cases of gastric ulcer. Instances have been recorded of the association with gastric ulcer of most of the diseases to which blood-vessels are subject. An example in all respects convincing of embolism of the artery supplying the ulcerated region of the stomach has not been published. Probably the best case belonging here is one of perforating ulcer of the stomach with hemorrhagic infiltration in its walls, presented by Janeway to the New York Pathological Society in 1871. In this case there was in the gastro-epiploic artery an ante-mortem fibrinous plug which was continued into the nutrient artery of the ulcerated piece of the stomach. No source for an embolus could be found. In one case Merkel found an embolus in a small artery leading to an ulcer {511} of the duodenum. The arch of the aorta was atheromatous and contained a thrombus. Patches of hemorrhagic infiltration existed in the stomach.

In many cases thrombosis of the arteries, and especially of the veins involved in the diseased tissue around an ulcer, has been observed, and in some the thrombus was prolonged in the vessels for a considerable distance from the ulcer. It is probable that in most of these cases the thrombus was secondary to the ulcer. Hyaline thrombosis of the capillaries near the ulcer is also to be mentioned.

In a certain, but not large, number of cases atheroma with calcification or with fatty degeneration of the arteries of the stomach has been found associated with gastric ulcer. Reference has already been made to the occurrence of obliterating endarteritis in the thickened edges and floor of gastric ulcer, where it is doubtless secondary. In one case of gastric ulcer I found a widespread obliterating endarteritis affecting small and medium-sized arteries in many parts of the body, including the stomach.

In one case Powell found a small aneurism of the coronary artery in an ulcer of the lesser curvature of the stomach. Hauser found an aneurismal dilatation of an atheromatous and thrombosed arterial twig in the floor of a recent ulcer. In my case of obliterating endarteritis just referred to there was a small aneurism in the floor of the ulcer. These miliary aneurisms in the floor of gastric ulcers seem to be analogous to those in the walls of phthisical cavities. Miliary aneurisms occur in the stomach independently of gastric ulcer, and may give rise to fatal hæmatemesis, as in four cases reported by Galliard.

Gastric ulcer is occasionally associated with waxy degeneration of the arteries of the stomach. In most of these cases there were multiple shallow ulcers. Hæmatemesis is generally absent in gastric ulcer resulting from waxy disease of the gastric blood-vessels. As is well known, the amyloid material itself resists the action of the gastric juice.

Finally, varicosities of the veins of the stomach have been once in a {512} while found with gastric ulcer. In a large number, probably in the majority, of cases of gastric ulcer no changes have been found in the blood-vessels of the stomach except such as were manifestly secondary to the ulcer.

That gastric ulcer is frequently complicated with chronic catarrhal gastritis has been repeatedly mentioned in the course of this article.

PATHOGENESIS.--Without doubt, the most obscure chapter in the history of gastric ulcer is that relating to its origin and to its persistence. Notwithstanding a vast amount of investigation and of discussion, unanimity of opinion upon these subjects has not been reached. In view of this uncertainty it is desirable in this article to do little more than to summarize the leading theories as to the development of gastric ulcer.

Most observers are agreed that the digestive action of the gastric juice has some share in the development and the progress of the ulcer, but as to the first cause of the ulcer there are various hypotheses.

The earliest theory refers the origin of simple ulcer of the stomach to inflammation. Since its advocacy by Abercrombie and by Cruveilhier this theory has always had its adherents, particularly among French writers. It is true that in stomachs which are the seat of simple ulcer evidences of inflammation can often be found both in the neighborhood of the ulcer and elsewhere. In recent times the supporters of the inflammatory origin of gastric ulcer lay especial stress upon the presence of foci of infiltration with small round cells in the mucous and the submucous coats. But it is difficult to explain by the inflammatory theory the usually solitary occurrence and the funnel-like shape of gastric ulcer.

The theory that gastric ulcer is of neurotic origin has also been advocated. Some refer the origin to the secretion of an excessively acid gastric juice under abnormal nervous influence (Günsburg), others to vaso-motor disturbances, and others to trophic disturbances. Wilks and Moxon compare simple gastric ulcer to ulcers of the cornea resulting from paralysis of the trigeminus. The neurotic theory of the origin of gastric ulcer is altogether speculative and has never gained wide acceptance.

The view which has met with the greatest favor is that which attributes the origin of gastric ulcer to impairment or arrest of the circulation in a circumscribed part of the wall of the stomach, and to a subsequent solution by the gastric juice of the part thus affected. Rokitansky first suggested this view by assigning hemorrhagic necrosis of the mucous membrane as the first step in the formation of the ulcer; but it is Virchow who has most fully developed this view and has given it its main support. The first cause of gastric ulcer, according to Virchow, is a hemorrhagic infiltration of the coats of the stomach induced by local disturbances in the circulation. The part the nutrition of which is thus impaired or destroyed is dissolved by the gastric juice.

{513} The affections of the gastric blood-vessels to which importance has been attached are (a) embolism and thrombosis; (b) diseases of the coats of the vessels, as atheroma, obliterating endarteritis, fatty degeneration, amyloid degeneration, and aneurismal and varicose dilatations; (c) compression of the veins by spasm of the muscular coats of the stomach in vomiting and in gastralgia; (d) passive congestion of the stomach by obstruction in the portal circulation.

In support of this view are urged the following facts: First, it has been proven by the experiments of Pavy that parts of the gastric wall from which the circulation has been shut off undergo digestion; second, hemorrhagic infarctions have been observed in the stomach, both alone (Von Recklinghausen, Hedenius) and associated with gastric ulcer (Key, Rindfleisch); third, the hemorrhagic infiltration in the walls of recently-formed ulcers indicates a hemorrhagic origin; fourth, the funnel-like shape of the ulcer resembles the funnel-shaped area of distribution of an artery; fifth, gastric ulcers have been experimentally produced by injecting emboli into the gastric arteries (Panum, Cohnheim).

The main objections to this view are the infrequency with which the assumed changes in the blood-vessels have been demonstrated, the common occurrence of gastric ulcer at an age earlier than that at which diseases of the blood-vessels are usually present, and the absence of gastric ulcer in the vast majority of cases of heart disease, with widespread embolism of different organs of the body. To meet some of these objections, Klebs presupposes in many cases a local spasmodic contraction of the gastric arteries, causing temporary interruption of the circulation; Rindfleisch and Axel Key, compression of the gastric veins, with resulting hemorrhagic infiltration by spasm of the muscular coat of the stomach in vomiting and in gastralgic attacks. But these are pure hypotheses.

What is actually known concerning diseases of the gastric blood-vessels in ulcer of the stomach has already been stated under the morbid anatomy. From this it may be inferred that the origin of gastric ulcer in diseased conditions of the blood-vessels has been established only for a comparatively small group of cases.

Böttcher's view that gastric ulcer is of mycotic origin, being produced by micrococci, has thus far met with no confirmation.

There are those who hold an eclectic view concerning the origin of gastric ulcer. They believe that ulcer of the stomach may be produced by a variety of causes, such as inflammation, circulatory disturbances, irritating substances introduced into the stomach, traumatism, etc. The peculiarities of the ulcer are due not to any specific cause, but to the solvent action of the gastric juice, which keeps clean the floor and the sides of the ulcer. These clean edges and floor, which are incident to all ulcers of the stomach, justify no conclusion as to the cause of the ulcer. Engel over thirty years ago held that gastric ulcer might {514} originate in various ways--that there was nothing specific about it. Brinton was also of similar opinion.